Using real-time PCR, we confirmed positive effects of PM inhalation on three distinct pathways: 1) up-regulation of CYP1A1, relevant to the presence of combustion by-products in the inhaled urban PM and activation of a procarcinogenic pathway; 2) up-regulation of metallothionein-II, relevant to the presence of toxic metals in the inhaled particles and activation of pathways to protect against metal toxicity and oxidative stress; and 3) up-regulation of ET-1, relevant to endothelial dysfunction generated by deposited toxicants and downstream cardiovascular effects. The gene discussed is MT2A; the disease is endothelial dysfunction.